Laminitis in Cattle

Laminitis is a pathophysiologic disturbance of the microstructure of the dermis or corium of the claw. The use of the term laminitis is misleading, as changes are not confined to the laminar region. Laminitis can be acute, subacute, chronic, or subclinical, depending on the variables involved.

Acute or Subacute Laminitis

Acute laminitis is not common in cattle and usually is seen in a single animal or a group that has accidentally engorged on large quantities of grain. The incidence of acute laminitis in dairy cattle probably varies from 0.6–1.2%. Subacute laminitis may be seen in young beef bulls on feeding trials and in feeder calves that have been fed rations rich in carbohydrates.

Clinical Findings

Acute and subacute laminitis have a rapid onset. In the most acute cases, there may be fever and an increased respiratory rate. In the initial phases, the claws may be warm to the touch, and a pronounced digital pulse will be perceptible. Pain may be detected in the claws with the use of hoof testers. The animal will be reluctant to walk and will stand abnormally with the feet drawn under the body. Frequently, the superficial veins of the hindlimbs will be turgid.

Treatment

If the cause is obvious, such as grain overload, it should be corrected. Keeping the animal moving and the claws cool are helpful. Antihistamines may be useful if given within the first 48 hr after a known insult. Anti-inflammatory drugs may be useful if given before the onset of acute signs. However, caution should be exercised in using corticosteroids later than 24 hr after signs appear.

Control

Because acute laminitis usually develops as the result of an accident, little can be done to prevent the condition.

Chronic Laminitis

Chronic laminitis is recognized by the bent, flat, square-toed, and heavily ridged appearance of the claw (slipper foot). It is the result of a prolonged process, and is assumed to be caused by a series of laminitic insults. It is most common in dairy cows >5 yr old.

Subclinical Laminitis

This form of laminitis is of considerable economic importance to the dairy industry as it predisposes mature cows to sole ulcer, white line disease, and toe ulcer. It has been seen in dairy cows in most developed countries and is of greatest concern in high-production, intensively managed herds.

Clinical Findings

There are no clinical signs. However, it appears that in any group of cows genetic predisposition to risk factors is variable. Therefore, presented with the same set of insults, a few cows may show signs of the subacute form of the disorder (see above). Some animals appear to walk in a deliberate, careful manner.

Hemorrhages in the sole and/or white line are consistent findings. If the appearance of sole and toe ulcers, white line disease, and double sole is >10% in the multiparous cows in a herd, it may be assumed that subclinical laminitis exists.

Erythema and edema (puffy foot) of the skin above the coronary band and around the dewclaws in freshly calved cows may indicate a transitory laminitis-like insult and that the cows are being introduced to concentrate too rapidly.

Etiology

The etiology of subclinical laminitis is incompletely understood. The classic hypothesis for the etiology of laminitis in cattle suggests that high levels of carbohydrate in the rumen invoke an increase of Streptococcus bovis and Lactobacillus spp, which induce a state of acidosis in the rumen. This causes gram-negative organisms to die and release vasoactive endotoxins. Rumenitis is frequently associated with ruminal acidosis. High levels of histamine in the blood have been found in the early stages of the disease. It is probable that subacute ruminal acidosis (SARA) is one key factor in development of laminitis, because managing SARA does help to control the incidence of subclinical laminitis (see Subacute Ruminal Acidosis).

Contemporary thinking is that as production levels increase, cows become more sensitive to risk factors. A risk factor is any physical insult causing stress. This probably leads to the release of bioactive messengers into the bloodstream. One important risk factor is trauma; many clinicians are convinced that hard flooring is equal in importance to nutritional problems. Care must be taken when dry cows and heifers are introduced to concrete after being accustomed to soft flooring. Prolonged standing, waiting in line to drink, or spending >3 hr in the holding yard each day are factors that are commonly overlooked. Social confrontation also causes stress. Unwillingness to lie down because of remembered discomfort is another reason for prolonged standing. On the other hand, inability to exercise reduces the amount of oxygen and nutrition delivered to the claw.

Pathogenesis

Although the release of biologic messengers into the bloodstream is known, identification of the agents that play a part in laminitis is ongoing. Epidermal growth factor (EGF) receptors are present in the basement membrane of the corium of the claw. EGF is liberated in large quantities from the GI tract when it is damaged (eg, rumenitis) and could be involved in the pathogenesis of laminitis. In addition to its mitogenic effect, EGF can inhibit the differentiation of keratinocytes in vitro. Inhibited differentiation of keratinocytes of the hoof matrix is a dominant morphologic feature in the early stages of laminitis. This supports the hypothesis that laminitic histopathology results from an inadequate regulation of gelatinase activity, resulting in selective degradation of basement membrane components and laminitis due to failure of the basement membrane-epidermis attachment.

More recent investigations have studied the role of matrix metalloproteinase (MMP) activity in the pathophysiology of laminitis. It is not known which endotoxins are involved in the etiology of laminitis. However, anecdotal reports from slaughterhouses have revealed that the incidence of liver abscesses in dairy cows can be greater than that found in beef steers. Fusobacterium necrophorum is regularly isolated from liver abscesses and, with its several biotypes, could provide the suspected endotoxins. Cytokines and prostaglandins may play a part, and certainly hypoxia has a role in accelerating the pathology. During the peripartum period, hormones such as relaxin are generated. Correct management of nutrition around calving is critical. In early calving heifers, it is possible that growth hormones could have a complicating role.

Whatever the biologic messengers, they appear to affect two different types of tissues: the papillary or solear dermis and the collagen fibers of the laminae. This results in two distinctly different pathologies. The first is disruption of normal keratogenesis, and the second, abnormal MMP activity, results in sinkage and/or rotation of the digit.

The pathophysiologic process associated with compromised horn production starts when vasoactive toxins or other biologic agents reach the corium. Arteriovenous shunts may be paralyzed, pressure inside the claw rises, and the walls of the vessels are damaged. Blood or blood fluids escape and soak into the claw horn, staining it either pink or yellow. Hemorrhagic staining of the horn tubules of the sole give a “brush mark” appearance. Mural thrombi form, reducing blood flow and causing oxygen deprivation and an insufficient nutrient supply to the keratin-producing cells. Thrombus formation is a characteristic feature of laminitis. The resulting horn is soft and prone to damage, infection, and scar formation.

The second pathophysiologic process involves MMP release and stretching of the collagen fibers of the suspensory apparatus of the digit. This is the system that transfers weight-bearing from the pedal bone to the inside wall of the claw. As the collagen fibers stretch, the pedal bone is displaced. Occasionally, the pedal bone will rotate and the apex of the bone will prolapse through the apex of the sole. Perhaps more frequently, the whole bone will “sink,” causing the space between the flexor process and the sole of the claw to narrow and increasing the possibility of a sole ulcer developing.

Frequently, young animals appear to recover from laminitis. This may be because new blood vessels develop to form collateral circulation and take over the function of those that have been damaged. Nevertheless, each time an animal has a bout of laminitis, more scar tissue is formed and the animal is less able to recover from the next insult.

Treatment and Control

Treatment for subclinical laminitis is impractical because diagnosis in an individual animal is not possible at the time of the causative insult(s). Controlling subclinical laminitis in a herd of high-production, intensively managed dairy cows requires a systematic epidemiologic study. The first step is to determine if any particular age group is more affected.

There appear to be many more problems in first-lactation animals than in any other group. It has been postulated that compromising the foot health of heifers reduces the animal's lifetime productivity. Heifers calving for the first time prior to 28 mo of age have a much higher incidence of lameness than those calving when they are older. In order for a heifer to calve at <24 mo of age, the young stock rearing protocols have to he changed. It is contraindicated for a heifer's average daily weight gain to exceed 750 g/day before she calves. This is particularly stressful for small-framed animals. Artificially accelerating puberty is another stressor.

Nutritional risk factors must be considered. Successfully managing SARA depends on the quantity and digestibility of the carbohydrate that is fed. The more rapidly carbohydrate is digested, the more rapidly rumen acidosis will develop. Finely ground or moist grains are more digestible than dry, cracked grain. Corn silage is frequently used in dairy production. Sometimes the energy content of the silage is completely underestimated, with disastrous results. Slug feeding once a day is contraindicated, and the more frequently concentrates are fed the better. Sudden changes in the diet or formulation of the diet are extremely dangerous. Component-fed cows should be given up to 7.5% of their body wt in concentrates around calving. After calving, it is safest if rations are not increased by more than 0.25 kg/day for multiparous cows and by 0.20 kg/day for primiparous cows to a maximum of 14–16 kg (30–36 lbs).

The quality and quantity of fiber fed is probably more important than the carbohydrate component of the diet. Fiber can, depending on its physical characteristics, stimulate rumination. If the carbohydrate:fiber ratio is >50% carbohydrate, the animal is increasingly at risk of rumenal acidosis. If the percentage of acid detergent fiber for the complete ration is <20%, risk of ruminal acidosis also increases. If the particle length of silage is cut too short (25% cut <5 cm long), the contribution of effective fiber is reduced. The manure should not contain fiber particles <1 cm or undigested grain. Feces should not contain mucin/fibrin casts, be foamy, or contain gas bubbles. The feces in the same feeding group should not vary from firm to diarrhea.

The Cow Comfort Index (CCI) is measured 1 hr before milking and calculated as the proportion of animals standing. If the CCI is >20%, risk factors affecting cow comfort should be reviewed. These include stall size, adequacy of bedding and bunk space, placement of water sources, and alley widths sufficient to avoid congestion or queuing. Time spent ruminating should be normal; rumen stasis and hypermotility should not be detectable.